MicroRNA-seq of cell lines expressing pri-miR-9 paralog constructs II
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA723320 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14287605.fastq.gz | Fastqsanger.gz | |||
| SRR14287606.fastq.gz | Fastqsanger.gz | |||
| SRR14287607.fastq.gz | Fastqsanger.gz | |||
| SRR14287608.fastq.gz | Fastqsanger.gz | |||
| SRR14287609.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 6 |
Similar Datasets
Project description:MicroRNA-seq of cell lines expressing pri-miR-9 paralog constructs
| PRJNA429035 | ENA
Project description:MicroRNA (miRNA) biogenesis begins with Drosha cleavage, the fidelity of which is critical for downstream processing and mature miRNA target specificity. To understand how pri-miRNA sequence and structure influence Drosha cleavage, we studied the processing of three pri-miR-9 paralogs (pri-miR-9-1, pri-miR-9-2 and pri-miR-9-3), which encode the same miRNA but differ in the surrounding scaffold. We show that pri-miR-9-1 has a unique Drosha cleavage profile due to its kinked tertiary structure. Cleavage of pri-miR-9-1, but not pri-miR-9-2 or pri-miR-9-3, generates an alternative-miR-9 with a shifted seed sequence that expands the scope of its target RNAs. Here, we report the the miRNA-seq data of HEK293T and HeLa cell lines transfected with different pri-miR-9 constructs.
2018-12-10 | GSE108893 | GEO
Project description:MicroRNA (miRNA) biogenesis begins with Drosha cleavage, the fidelity of which is critical for downstream processing and mature miRNA target specificity. To understand how pri-miRNA sequence and structure influence Drosha cleavage, we studied the processing of pri-miR-9-1 sequence variants, which encode the same mature miRNA but differ in the surrounding scaffold. We show that, in addition to previously known features, the overall structural flexibility of pri-miRNA impacts Drosha cleavage fidelity. Internal loops and nearby G·U wobble pairs on the pri-miRNA stem induce the use of non-canonical cleavage sites by Drosha, resulting in 5’ isomiR production. Here, we report the the miRNA-seq data of HEK293T cell lines transfected with different pri-miR-9 constructs.
2022-01-27 | GSE172446 | GEO
Project description:MicroRNAs (miRNAs) are short non-coding RNAs that play essential roles in RNA silencing and gene regulation. The human Microprocessor (MP) is the key factor to initiate miRNA biogenesis by cleaving primary microRNAs (pri-miRNAs). However, the Microprocessor alone cannot precisely and efficiently cleave all pri-miRNAs; thus, it requires cofactors to assist its cleavage. SRSF3 interacts with CNNC in pri-miRNAs, enhancing the MP cleavage. However, it is unknown if SRSF3 can function with other non-CNNC motifs and if secondary structure might influce CNNC function. In addition, function of SRSF7, a paralog of SRSF3, in the SR proteins family, in miRNA biogenesis is largely unknown. In this study, by conducting the high-throughput pri-miRNA cleavage assays for the MP with SRSF3 or SRSF7 and randomized pri-miRNAs, we discovered that SRSF7 also stimulate MP clevage. Futhermore, we found that both SRSF3 and SRSF7 can function with some non-CNNC motifs and with CNNC motifs with certain secondary structures. Furthermore, we also demonstrated that SRSF7 and SRSF3 governed the cleavage sites of the Microprocessor in human cells. Our findings disclose the roles SRSF7 in miRNA biogenesis, demonstrate a compresenhive moleucalr mechanism of SFSF3 and SRSF7 in enhancing cleavage of MP and described in more detail the RNA-binding features of SRSF7 and SRSF3.
2023-01-23 | GSE221996 | GEO
Project description:This project was aimed to identify the proteomic of pri-miR-31 interacting in naïve and activated cd4+ T cells. Immunoprecipitates pulled down by pri-miR-31 were subjected to LC-MS. Our results reveal the interacting protein in different state of CD4+ T cells.
2024-06-24 | PXD038182 | Pride
Project description:Human Microprocessor cleaves pri-miRNAs to initiate miRNA biogenesis. The accuracy and efficiency of Microprocessor cleavage ensure appropriate miRNA sequence and expression and thus its proper gene regulation. However, Microprocessor cleaves many pri-miRNAs incorrectly, so it requires assistance from its many cofactors. For example, SRSF3 enhances Microprocessor cleavage by interacting with the CNNC motif in pri-miRNAs. However, whether SRSF3 can function with other motifs and/or requires the motifs in a certain secondary structure is unknown. In addition, the function of SRSF7 (a paralog of SRSF3) in miRNA biogenesis still needs to be discovered. Here, we demonstrated that SRSF7 could stimulate Microprocessor cleavage. In addition, by conducting high-throughput pri-miRNA cleavage assays for Microprocessor and SRSF7 or SRSF3, we demonstrated that SRSF7 and SRSF3 function with the CRC and CNNC motifs, adopting certain secondary structures. In addition, SRSF7 and SRSF3 affect the Microprocessor cleavage sites in human cells. Our findings demonstrate the roles of SRSF7 in miRNA biogenesis and provide a comprehensive view of the molecular mechanism of SRSF7 and SRSF3 in enhancing Microprocessor cleavage.
2023-01-23 | GSE215790 | GEO
Project description:Menin, the product of the MEN1 gene in humans (Men1 in mice), is responsible for the inherited tumor syndrome, multiple endocrine neoplasia type 1 (MEN1). menin interacts with the trithorax group (trxG) proteins (Drosophila) and the mixed-lineage leukemia (MLL) (humans) histone methyltransferase (HMTase) complex, and it alters histone tail modifications and the transcription of target genes. To explore a potential functional implication of menin in HCC, we stably transfected HepG2 or L-02 cells with either vectors or constructs expressing MEN1. A cDNA microarray analysis was performed on HepG2 or L-02 cells with either vectors or constructs expressing MEN1. To obtain a broader understanding of the molecular network of menin in HCC, the whole genome microarray expression profiling was performed on HepG2 or L-02 cells with either vectors or constructs expressing MEN1.
2015-07-07 | GSE70556 | GEO
Project description:Menin, the product of the MEN1 gene in humans (Men1 in mice), is responsible for the inherited tumor syndrome, multiple endocrine neoplasia type 1 (MEN1). menin interacts with the trithorax group (trxG) proteins (Drosophila) and the mixed-lineage leukemia (MLL) (humans) histone methyltransferase (HMTase) complex, and it alters histone tail modifications and the transcription of target genes. To explore a potential functional implication of menin in HCC, we stably transfected HepG2 or L-02 cells with either vectors or constructs expressing MEN1. A cDNA microarray analysis was performed on HepG2 or L-02 cells with either vectors or constructs expressing MEN1. To obtain a broader understanding of the molecular network of menin in HCC, the whole genome microarray expression profiling was performed on HepG2 or L-02 cells with either vectors or constructs expressing MEN1. Comparison of gene expression results from HepG2 or L-02 cells with either vectors or constructs expressing MEN1.
2015-07-07 | E-GEOD-70556 | biostudies-arrayexpress
Project description:The microRNAs encoded by the miR-17~92 polycistron are commonly overexpressed in cancer and orchestrate a wide range of oncogenic functions. Here, we identify a novel mechanism for miR-17~92 oncogenic function through the disruption of endogenous miRNA processing. We show that upon oncogenic overexpression of the miR-17~92 primary transcript (pri-miR-17~92), the Microprocessor complex remains associated with partially processed intermediates that aberrantly accumulate. These intermediates reflect a series of hierarchical and conserved steps in the early processing of the pri-miR-17~92 transcript. Encumbrance of the Microprocessor by miR-17~92 intermediates leads to the broad, but selective, downregulation of co-expressed polycistronic miRNAs, including miRNAs derived from tumour suppressive miR-34b/c, and from the Dlk1-Dio3 polycistrons. We propose that the newly identified steps of polycistronic miR-17~92 biogenesis contribute to the oncogenic re-wiring of gene regulation networks. Our results reveal new functional paradigms for polycistronic miRNAs in cancer.
2019-05-20 | GSE130282 | GEO